Test 2 Flashcards

1
Q

Dendritic Spine

A

a small bud on the surface of a dentrite that the terminal button of another neuron attaches to making a synapse

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2
Q

Presynaptic membrane and postsyanptic membrane

A

presynaptic membrane is located on the terminal button and faces the postsynaptic membrane which is located on the neuron recieving the message

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3
Q

Synaptic Cleft

A

the gap between the pre and post synaptic membranes of two neurons

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4
Q

3 types of synapses

A
  1. Axondendritic synapes; occur on smooth surface of dendrite and on dendrite spine (both with termnial button)
  2. Axsomatic synapses: occur on the somatic membrane with termnial button
  3. Axoaxonic synapses: occur between two termnial buttons
    1 and 2 effect postsynapse (either postsynaptic facilitation or postsynaptic inhibitiation)
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5
Q

Two Types of Receptors for Synapses

A

Direct and Indirect
1. Ionotropic receptor: is direct; neurotransmitters talk with this receptor which has a binding site for the NT’s and a ion channel. The channel opens when the NT’s connect with the neurons binding site; THIS IS FAST AND DIRECT
2. Metabotropic Receptor: Indirect; takes longer but lasts longer; needs metabolic energy to open ion channel; is a receptor within a neuron that when connected with a molecule of an NT it produces a second messenger which then opens the ion channel
This receptor is located closely to G-proteins which is activated when molecule of NT connects with receptor and creates an enzyme that creates the second messenger.

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6
Q

G-Protein

A

next to metabotropic receptors that when activated, create a chemical called the second messenger.

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7
Q

Second messenger

A

a chemical produced by the enzyme in a G-protein. When produced this chemical allows for ion channels to be opened within a neuron

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8
Q

Autoreceptor

A

self; a receptor molecule on a neuorn that responds to its own the neurotransmitter
IS LIKE A THERMOSTAT, turns off the production and release of neurotransmitters if there are too many; do not produce change in membrane potential because they are not in control of ion channels; REGULATE SYTHESIS AND NEUROTRANSMITTER PRODUCTIONS

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9
Q

Neuromodulator

A

is like a NT but it is not restricted to the synaptic cleft; but travels through the extracellular fluid; CAN GO FAR
Most are peptides

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10
Q

Peptides

A

a in neuromodulators and some hormones; is a chain of amino acids joined together by peptide bonds

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11
Q

site of action

A

place where drugs effect certain molecules within our body and thus cause some biochemical change

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12
Q

Pharmacokinectics

A

the movement of drugs within the body

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13
Q

Gap Junctions

A

pruely electrical synapes
more neurons without NT’s
are immediate
not modiable (more reflexsive)

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14
Q

Tolerance

A

drug becomes less effective; need more and more to get the same resutl

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15
Q

Sensitivity

A

drug becomes more effective; need less and less to get the same result

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16
Q

Withdrawal

A

effects when a drug is administered repeatedly and then taken away

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17
Q

Two types of drugs

A

antagonist: drugs that block or inhibit postsynaptic effects
agonists: drugs that increase or facilitate postsynaptic effects

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18
Q

Effect of Drugs on Production of Neurotransmitters

A

the synthesis is conotrolled by enzymes; so when drug inactivites one of these enzymes it will prevent the neurotransmitter from being produced; drug serves as an antagoinist

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19
Q

Effect of Drugs on Storage and Release of Neurotransmitters

A

Drugs act as antagonist is storage of NT’s by binding to transporter molecules which are incharge of filling vesicles with NT’s
Drugs act as antagonist and agonists with the release of NT’s from the terminal button; they deactive or activate proteins that make vesicles fuse with presynaptic membrane and expell them into the synaptic cleft

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20
Q

Effect of Drugs on Receptors

A

MOST IMPORTANT EFFECT ON NERVOUS SYSTEM BY DRUGS
Postsynpatic Receptors: can be affected by drugs as antagonist or agonists; the drugs attach to the postsynaptic receptor just as NT’s do, which blocks NT’s from connecting. When connected the drug can act as direct antagonist and not allow ion channels to open or it can act as an direct agonist and cause the ion channels to open
OR can be a noncompetitive binding situation in which the same actions occur but NT’s are still allowed to bind to recptors but the Recport is still controlled by drugs being indirect antagonist or indirect agonists

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21
Q

Noncompetitive Binding

A

when a postsynapic receptor has multiple binding sites and thus the NT’s and other modulators or drugs do not have to compete to bind; receptor becomes either a indirect antagonist or indirect agonist depending on what the drug does

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22
Q

Effect of Drugs on Reuptake and Destruction

A

Reuptake is when the NT’s are taken back up and reused; Destruction is when NT’s are destroyed by enzymes
REUPTAKE: drugs can attach to transporter molecules that move the NT’s back into terminal button with reuptake, when they attach they make the molecule inactive and thus block reuptake
DESTRUCTION: drugs bind with enzyme that destroys NT’s and makes it inactive and thus blocks destruction

23
Q

Agonist

A

add neurotransmitters, block reuptake, block autoreceptors, block metabolic energy

24
Q

antagonists

A

block sythesis, blocking agent, block release of vesicles, stimulate autoreceptors

25
Q

Acetylcholine

A

primary neurotransmitter secreted by efferent axons in the CNS; is found in and out of the CNS ; is involved in all muscular movement; composed of choline and acetate; IS INVOLVED IN REM SLEEP AND LEARNING AND MEMORY

26
Q

Biosynthesis of Acetylcholine

A

Inolves Acetyl coenzyme A and Choline acetyltransferse which make acetylcholine

27
Q

Acetyl-COa

A

cofactor that supplices acetate for teh synthesis of acetylcholine

28
Q

Choline acetyltransferse

A

transfers the acetrate ion from acetyl-coenzyme a to choline

29
Q

Monoamines (4)

A

dopamine, norepinephrine, epinephrine and serotonin

30
Q

2 prinicipels of Drugs and NT systems

A
  1. they never create new effects, just modify effects already present
  2. Drug x is 99% reliant on albumen, when drug y comes in it competes for this and takes up space which frees up drug x, making it more potent WHEN TO DRUGS ARE USED LIKE ALCOHOL AND WEED
31
Q

Cholinergic Receptors (2)

A

Nicotinic and muscarinic; these are responsible for the addictive effects of the drug nicotine

32
Q

Nicotinic Receptor

A

is agonist; is ionotropic acetylcholine receptor that is stimulated by nicotine and blocked by curare; must bind with antagonist to create competitive blocking agent-curare
Increase heart rate, is incharge of fight or flight; increases vigilance and attension

33
Q

Muscarinic receptor

A

is a metabotropic acetylcholine that is stimulated by muscarine and blocked by atropine; descreases heart rate, is hallucinogenic, involved in rem sleep, comes from mushrooms, pupils dialate

34
Q

Curare

A

blocks nicotine receptors; causes paralysis; very fast, paralizes muscles

35
Q

Atropine

A

increases heart rate, is a competative blocker, dialates pupils, fever, blocks muscarinic acetylcholine receptors

36
Q

Black Widow SPider and Boutilin Toxin

A

BWS releases acetylcholine

Boutilin Toxin prevents release of acetylcholine

37
Q

Dopamine

A

involved in movement, reward/ pleasure, attension

Is a catecholamine

38
Q

Synthesis of Catecholamine

A

tyrosine (an amino acid) is converted by an enzyme to into I-DOPA, which is converted by another enzyme to Dopamine, dopamine is either used or converted again into norepinephrine

39
Q

Cocaine and Meth with Dopamine

A

are both agonists of dopamine

Cocaine blocks reuptake and meth induces release of dopamine

40
Q

Amino Acid Neurotransmitters

A
  1. GABA- Inhibitory NT, is produced from glutamic acid by an enzyme removing carboxyl group; has two receptors GABAa and GABAb
  2. Glutamate-excitatory NT; involved with learning and memory; created by the cells metabolic processes; four receptors are NMDA,AMPA, Kainate, and the Metabotropic Glutamate
41
Q

GABA two types of receptors

A

GABAa -is ionotropic and controls the chloride channels

GABAb -is metabotropic and controls the potassium channels

42
Q

Glutamate four receptors

A

the Metabotropic Glutamate, NMDA, AMPA, and Kainate

Last three are ionotropic

43
Q

5 Drug Treatmetns for Depression

A
  1. SSRI- agonist of serotonin
  2. Tricyclic Anti -immipramine which blocks reuptake of noreinephrine
  3. SSNRI-effexor
  4. MAO-Inhibitor
  5. COMI inhibitor
44
Q

Non-Drug Treatments for Depression

A
  1. Deep brain stimulation
  2. Transcarnial Magnetic Stimulation
  3. Electro convolsive Therapy
45
Q

Schizophrenia

A

Positive symptoms hallucinations and delusions

Negaitve symptoms flat affect, social withdrawal, disordered thought and cognition

46
Q

Dopamine Overactivity

A

1 meth addicts (DA agonist)

2. Atypical Antipsychotics

47
Q

Depression

A

associated with lower noreinephrine and lower serotonin

trypotphan depletion

48
Q

Peptides

A

are two or more amino acids linked together by peptide bonds
Most common is endogenous opioids
Effects are
1. constipate
2. Analgesic (takes away pain)
3. Pleasure- eurphoric and makes you sleepy

49
Q

Endogenous Opioids

A
  1. Endorphins binds to M receptor
  2. Enkephalins binds to (delta) receptor
  3. Dynorphins binds to kappa receptor
50
Q

Opioid Use vs Opioid Withdrawal

A

Withdrawal has the exact opposite effects to use
use: heart rate goes down, pupils constricted, body temperature goes down, sedative euphoric, analgesia (takes awya pain)

51
Q

Old and Milner

A

conducted a study in which rats would press a button which caused eletrical stimulation into their brain. The electrical stimulation was reinforcing and thus they continued the action

52
Q

Reinforcement

A

Dopamine is the most importnat NT
the most important places of dopamine are located in the ventral tegmental area and their axons project to the nucleus accumbens.

53
Q

Microdialysis

A

type of studies that have shown that natural and articifical stimulation cause the release of dopamine in the nucleus accumbends